CIC-2塩化物チャネルの開通に関与する地域は,電圧とセル容量による

S Gründer¹, A Thiemann, M Pusch

¹Centre for Molecular Neurobiology (ZMNH), Hamburg University, Germany.

Nature

|December 24, 1992

まとめ

細胞体積調節に不可欠なCIC-2塩化チャネルは,低圧性によって活性化され,広範な生理学的役割を果たしていることを示しています. その電圧と体積の活性化ドメインは,アミノ末端に位置しています.

科学分野:

細胞生物学細胞生物学
イオンチャンネル生理学イオンチャンネル生理学
分子生物学は分子生物学である.

背景:

細胞容量の調節は,細胞機能にとって不可欠であり,しばしばイオンとオスモライトの輸送を伴う.
クロライドチャネルは,規制容量の減少において重要な役割を果たします.
容量活性化塩化物流におけるP-グリコタンパク質の生理学的役割は不明である.

研究の目的:

細胞体積調節におけるCIC-2塩化チャネルの役割を調査する.
細胞外低圧性によるCIC-2の活性化メカニズムを決定する.
CIC-2の電圧とトニシティによる活性化に責任のある機能ドメインを特定する.

主な方法:

CIC-2チャネル活動を評価するための電気生理学的記録.
機能ドメインを特定するためのサイト指向型変異性.
細胞系における野生型および変異CIC-2の発現.

主要な成果:

CIC-2チャネルは細胞外低圧性によって活性化され,細胞体積調節における役割を示唆しています.
アミノ末端内の特定のドメインは,電圧および体積に依存する活性化に不可欠です.
"本質的な"領域の変異は,構成的に開かれたチャネルを生じ,一方"調節"領域の削除は,部分的に開かれたチャネルを生じます.

結論:

CIC-2は,細胞容量のホメオスタシスに重要な役割を果たす,至るところに発現する塩化物チャネルです.
CIC-2のアミノ末端には,電位と細胞外トニシティの変化の両方によって活性化するための重要なドメインが含まれています.
CIC-2の機能ドメインは操作され,刺激に対する反応で可塑性を示すことができる.

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